Evidence map›Paper›PMID 33536762›Full record

ArticleOncoTargets and therapy2021

CPNE1 Enhances Colorectal Cancer Cell Growth, Glycolysis, and Drug Resistance Through Regulating the AKT-GLUT1/HK2 Pathway.

Yuexia Wang, Shengli Pan, Xinhong He, Ying Wang, Haozhe Huang, Junxiang Chen, Yuhao Zhang, Zhijin Zhang, Xianju Qin

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Cpne1 deficiency preserves sperm motility under CaThe Journal of reproduction and development · 2024
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  9. Review
  10. The PI3K/Akt Pathway and Glucose Metabolism: A Dangerous Liaison in Cancer.International journal of biological sciences · 2024
    Review
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  18. Article
  19. Review
  20. PBX1: a key character of the hallmarks of cancer.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Yuexia Wang *Department of General Surgery, Shanghai Eighth People's Hospital, Jiangsu University, Shanghai, People's Republic of China.
Shengli Pan *Department of General Surgery, Shanghai Eighth People's Hospital, Shanghai, People's Republic of China.
Xinhong HeDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China.
Ying WangDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China.
Haozhe HuangDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China.
Junxiang ChenDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center, Shanghai, People's Republic of China.
Yuhao ZhangDepartment of General Surgery, Shanghai Eighth People's Hospital, Shanghai, People's Republic of China.
Zhijin ZhangDepartment of General Surgery, Shanghai Eighth People's Hospital, Shanghai, People's Republic of China.
Xianju QinDepartment of General Surgery, Shanghai Eighth People's Hospital, Shanghai, People's Republic of China.ORCID 0000-0002-8206-0335
Shanghai Eighth People Hospital · CNFudan University Shanghai Cancer Center · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionColorectal cancer (CRC) is a major cause of cancer-related mortality worldwide. Copines-1 (CPNE1) has been shown to be overexpressed in various cancers; however, the role of CPNE1 in CRC remains unknown. Therefore, it is of great importance to elucidate the role of CPNE1 in CRC and its underlying mechanism of action.

methodsCPNE1 expression in CRC tissues was measured by quantitative real-time PCR and immunohistochemical (IHC) staining. CPNE1 was knocked down (KD) or overexpressed using small inferring RNAs or lentiviral transduction in CRC cells. The proliferation, apoptosis, glycolysis, and mitochondrial respiration of CRC cells were assessed by cell counting kit-8, flow cytometry, and Xfe24 extracellular flux analyzer assays, respectively. The role of CPNE1 in tumor growth and chemoresistance was further confirmed in xenograft and patient-derived tumor xenograft models, respectively.

resultsCPNE1 mRNA and protein were upregulated in CRC tissues. CPNE1 promoted proliferation, inhibited apoptosis, increased mitochondrial respiration, enhanced aerobic glycolysis by activating AKT signaling, upregulated glucose transporter 1 (GLUT1) and hexokinase 2 (HK2), and downregulated the production of cleaved Caspase-3 (c-Caspase 3). CPNE1 also contributed to chemoresistance in CRC cells. CPNE1 KD inhibited tumor growth and increased the sensitivity of tumors to oxaliplatin in vivo.

conclusionCPNE1 promotes CRC progression by activating the AKT-GLUT1/HK2 cascade and enhances chemoresistance.

Indexed as

aerobic glycolysiscolorectal cancercopines-1mitochondrial respiration

Identifiers

PMID33536762
PMCPMC7850573
OpenAlexW3123227540

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.